NBME Free 150 Discussion (spoilers)

[doctoritis]

I can't seem to find explanations anywhere, most of these questions are cake and I know this is supposed to easy ... but I do have a few questions. I'll just post some of the ones i'm struggling on, any help in understanding them would be appreciated. Thank you!

(http://www.usmle.org/pdfs/step-1/2013content_step1.pdf)


1. 45 year old women who has progressive SOB, not a smoker. Her vital capacity is at 60%, FEV1 is at 70%, CO diffusing capacity is at 50%, maximum voluntary ventilation is at 60%.

What explains her limited ventilation?
-> airway obstruction, decreased activation of pulmonary juxtacapillary receptors, decreased lung compliance, depression of central chemoreceptors, depression of peripheral chemoreceptors

(answer is decreased lung compliance -> but how do we know it is this and not airway obstruction?)



2. A comatose man is intubated after a motorcycle collision, he dies, they give you a picture of tracheal tissue obtained after biopsy and ask you for what type of process has happened. The answer is metaplasia -> i mean that was my gut instinct, but i actually have no clue how i was supposed to know that ... versus like hyperplasia, hypertrophy, dysplasia?




3. the woman who ingested aspirin in a suicide attempt - she presents 3 hours after ingestion. and they ask you for her HCO3, pH and pCO2 values. (answer: low bicarb, low pH, low CO2)
NOW - i get that here she is in an metabolic acidosis, and therefore you pick the values accordingly. she also has an increased respiration rate so she's blowing off some CO2. --> i feel like that would be my gut reaction to this question, but UWorld totally confused me about aspirin over dose with saying that initially you see a "respiratory alkalosis" and then only later is it a "metabolic acidosis", 3 hours into an ingestion is pretty early and i think that Uworld question was at something like 5 hours, so why are we seeing a metabolic acidosis and not a respiratory alkalosis here?!?!

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[rueby25]

I can't seem to find explanations anywhere, most of these questions are cake and I know this is supposed to easy ... but I do have a few questions. I'll just post some of the ones i'm struggling on, any help in understanding them would be appreciated. Thank you!

(http://www.usmle.org/pdfs/step-1/2013content_step1.pdf)


1. 45 year old women who has progressive SOB, not a smoker. Her vital capacity is at 60%, FEV1 is at 70%, CO diffusing capacity is at 50%, maximum voluntary ventilation is at 60%.

What explains her limited ventilation?
-> airway obstruction, decreased activation of pulmonary juxtacapillary receptors, decreased lung compliance, depression of central chemoreceptors, depression of peripheral chemoreceptors

(answer is decreased lung compliance -> but how do we know it is this and not airway obstruction?)


2. A comatose man is intubated after a motorcycle collision, he dies, they give you a picture of tracheal tissue obtained after biopsy and ask you for what type of process has happened. The answer is metaplasia -> i mean that was my gut instinct, but i actually have no clue how i was supposed to know that ... versus like hyperplasia, hypertrophy, dysplasia?


3. the woman who ingested aspirin in a suicide attempt - she presents 3 hours after ingestion. and they ask you for her HCO3, pH and pCO2 values. (answer: low bicarb, low pH, low CO2)
NOW - i get that here she is in an metabolic acidosis, and therefore you pick the values accordingly. she also has an increased respiration rate so she's blowing off some CO2. --> i feel like that would be my gut reaction to this question, but UWorld totally confused me about aspirin over dose with saying that initially you see a "respiratory alkalosis" and then only later is it a "metabolic acidosis", 3 hours into an ingestion is pretty early and i think that Uworld question was at something like 5 hours, so why are we seeing a metabolic acidosis and not a respiratory alkalosis here?!?!

1)This is getting you to recognize obstructive vs. restrictive lung disease. By virtue of the increased fev1/fvc ratio, this is restrictive.

2) other than knowing that carcinogens/irritants are likely to cause metaplasia, I would guess that knowing the tissue type that lines the trachea (I assume squamous epithelium, but it's been a while) then identifying what I assume to be cuboidal or another tissue type. This is a classic question for Barrett's esophagus and chronic GERD.

3) don't over think it. Aspirin OD is a mixed respiratory alkalosis with a metabolic acidosis. Yes 3 hours is relatively short... But when they say short, they mean minutes.

Hope this helps.

 

[g8orlife]

1)This is getting you to recognize obstructive vs. restrictive lung disease. By virtue of the increased fev1/fvc ratio, this is restrictive.

2) other than knowing that carcinogens/irritants are likely to cause metaplasia, I would guess that knowing the tissue type that lines the trachea (I assume squamous epithelium, but it's been a while) then identifying what I assume to be cuboidal or another tissue type. This is a classic question for Barrett's esophagus and chronic GERD.

3) don't over think it. Aspirin OD is a mixed respiratory alkalosis with a metabolic acidosis. Yes 3 hours is relatively short... But when they say short, they mean minutes.

Hope this helps.

Right. OP, remember that ASA uncouples the ETC which causes less ATP. In order to make up for the inefficient ETC, the body instead increases the frequency/rate of the ETC. Since the ETC uses/needs oxygen, we hyperventilate to increase the amount of oxygen in the body. This happens quickly and we see the respiratory alkalosis.
That's phase 1 of ASA toxicity.

Phases 2 + 3 involve aciduria + metabolic acidosis which begin within hours.